Genetic recombination is an essential feature of normal meiosis and during repair of various types of DNA damage. As part of a program to understand the mechanisms of recombination and its genetic control, the timing and the location of recombination events are being evaluated by applying modeling procedures to biochemical data. DNA lesions are used as markers in exchange processes where the lesions can be identified using enzymes which will nick the DNA, and thus reduce the size of the DNA. If recombination occurs, lesions induced in parental strands of DNA can become associated with newly synthesized DNA; therefore, as a result of recombination events, newly synthesized DNA can become sensitive to nicking enzymes. Using this approach, we have been able to predict, by mathematical modeling, the detectibility of exchanges knowing the average number of lesions per parental molecule. Analysis of results with E. coli indicates that every unrepaired dimer (induced by UV) causes a reciprocal exchange event. Results with yeast undergoing meiosis or during mitotic growth indicate that DNA damage is very inefficient at causing reciprocal exchange events; similar conclusions can be drawn for mammalian cells.